Differential effects of dopamine on glucoregulatory hormones in rats

Keck, F. S.; Foldenauer, Ann Christina; Wolf, CF; Zeller, Geraldine C.; Meyerhoff, C; M, Dolderer; Loos, U.; Pfeiffer, Ernst-Friedrich

doi:10.1016/0168-8227(90)90026-p

Cited by 5 publications

(2 citation statements)

References 15 publications

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“…In contrast to norepinephrine, which predominantly activates α-adrenergic receptors, dopamine concentration-dependently stimulates β-and α-adrenergic receptors, thereby influencing glucose homeostasis in a concentrationdependent manner. While low dopamine concentrations (<15 µg/kg per minute) do not influence serum glucose levels and insulin release, high concentrations (60 µg/kg per minute) mediated via α-adrenergic receptors significantly increase serum glucose and decrease serum insulin levels in uninjured rats [34]. When carefully transferred to the present study -as judged by the measured plasma glucose levels -it appears as if the infused dopamine concentrations in these brain-injured rats were not within the range known significantly to reduce insulin secretion via activation of α 2 -adrenergic receptors as seen for norepinephrine.…”

Section: Discussionmentioning

confidence: 99%

Norepinephrine-induced hyperglycemia does not increase cortical lactate in brain-injured rats

Stover

Sakowitz

Thomale

et al. 2002

Intensive Care Medicine

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Norepinephrine and dopamine significantly increased pericontusional glucose concentrations which did not elevate extracellular lactate and aggravate underlying posttraumatic edema formation. In addition to possibly increased facilitated endothelial glucose transport, the elevated extracellular to blood glucose ratio suggests a passive concentration- and pressure- dependent entry via a damaged blood-brain barrier. This might contribute to the observed reversible increase in extracellular glucose.

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Section: Discussionmentioning

confidence: 99%

Norepinephrine-induced hyperglycemia does not increase cortical lactate in brain-injured rats

Stover

Sakowitz

Thomale

et al. 2002

Intensive Care Medicine

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show abstract

“…Pivotal studies suggested that intravenous dopamine infusion stimulated glucagon release [32] in a dose-dependent manner [33]. Keck et al found that low-dose dopamine (e.g., 2 mcg/kg/min infused for 6 consecutive hours) did not affect both insulin and glucagon secretion [34], but high-dose dopamine was found to provide relevant hyperglycemia by suppressing insulin and stimulating glucagon secretion in rats and men [32,33]. The effect could be considered an additive mechanism by which dopamine and dopamine agonists could sustain hyperglycemia in healthy and T2D patients.…”

Section: The Effects Of Dopamine On Pancreatic Islets and Insulin And...mentioning

confidence: 99%

Dopamine in the Regulation of Glucose Homeostasis, Pathogenesis of Type 2 Diabetes, and Chronic Conditions of Impaired Dopamine Activity/Metabolism: Implication for Pathophysiological and Therapeutic Purposes

Lisco,

De Tullio,

Iovino

et al. 2023

Biomedicines

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Dopamine regulates several functions, such as voluntary movements, spatial memory, motivation, sleep, arousal, feeding, immune function, maternal behaviors, and lactation. Less clear is the role of dopamine in the pathophysiology of type 2 diabetes mellitus (T2D) and chronic complications and conditions frequently associated with it. This review summarizes recent evidence on the role of dopamine in regulating insular metabolism and activity, the pathophysiology of traditional chronic complications associated with T2D, the pathophysiological interconnection between T2D and chronic neurological and psychiatric disorders characterized by impaired dopamine activity/metabolism, and therapeutic implications. Reinforcing dopamine signaling is therapeutic in T2D, especially in patients with dopamine-related disorders, such as Parkinson’s and Huntington’s diseases, addictions, and attention-deficit/hyperactivity disorder. On the other hand, although specific trials are probably needed, certain medications approved for T2D (e.g., metformin, pioglitazone, incretin-based therapy, and gliflozins) may have a therapeutic role in such dopamine-related disorders due to anti-inflammatory and anti-oxidative effects, improvement in insulin signaling, neuroinflammation, mitochondrial dysfunction, autophagy, and apoptosis, restoration of striatal dopamine synthesis, and modulation of dopamine signaling associated with reward and hedonic eating. Last, targeting dopamine metabolism could have the potential for diagnostic and therapeutic purposes in chronic diabetes-related complications, such as diabetic retinopathy.

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The effects of dopamine infusion on the postoperative energy expenditure, metabolism, and catecholamine levels of patients after esophagectomy

et al. 1994

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Although dopamine is one of the most widely used vasoactive agents, its postoperative thermogenic and metabolic effects have not been studied. In this study, the effects of low-dose dopamine, given at 5 microgram/kg/min, on resting energy expenditure (REE), metabolism, and plasma catecholamine levels were examined in eight postsurgical patients. Dopamine infusion increased REE from 1,839 +/- 171 kcal/day to 2,071 +/- 170 kcal/day, and it decreased to 1,867 +/- 141 kcal/day after cessation of the infusion. Dopamine also increased the plasma levels of glucagon from 109.4 +/- 8.7 pg/ml to 132.5 +/- 8.0 pg/ml, and it decreased to 102.9 +/- 11.1 pg/ml after cessation of the infusion. The plasma levels of dopamine before, during, and after the infusion were 116.1 +/- 18.3, 161.1 +/- 25.6 and 121.4 +/- 17.2 ng/ml, respectively. Insulin and glucose were affected by dopamine, but changes in their plasma levels did not parallel the dopamine levels. Epinephrine and norepinephrine were increased by the infusion of dopamine and continued to increase even after its cessation. The results of this study revealed that low-dose dopamine increased REE in postsurgical patients and that this might be associated with the concomitant increase in plasma glucagon.

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Differential effects of dopamine on glucoregulatory hormones in rats

Cited by 5 publications

References 15 publications

Norepinephrine-induced hyperglycemia does not increase cortical lactate in brain-injured rats

Norepinephrine-induced hyperglycemia does not increase cortical lactate in brain-injured rats

Dopamine in the Regulation of Glucose Homeostasis, Pathogenesis of Type 2 Diabetes, and Chronic Conditions of Impaired Dopamine Activity/Metabolism: Implication for Pathophysiological and Therapeutic Purposes

The effects of dopamine infusion on the postoperative energy expenditure, metabolism, and catecholamine levels of patients after esophagectomy

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